1
Q
environmental history
A
Activities community household hobbies occupation oral behaviors
2
Q
Why are fetus/children most vulnerable?
A
toxins cross placenta rapid state of growht/development different absorption, metabolism unique habits/eat and drink, breathe faster longer life span
3
Q
Restrictive lung disease
A
reduction in TLC on PFTS from Lung disease that result in decreased compliance (decreased volumes) and extra pulmonary restriction limiting ability to generate negative pleural pressure
4
Q
Restriction due to lung disease
A
Lower compliant lungs (at any given pressure, lung volume will be less)
less compliant chest wall (any given pressure, lung volume less)
weakness (lower maximal inspiratory pressure-going to have a lower TLC)
5
Q
Restrictive lung disease PFTS CW
A
lower TLC, lower RV, normal/low DLCO (lungs are fine)
6
Q
Restrictive lung disease lung parenchyma
A
lower TLC, lower RV, super low DLCO
7
Q
Restrictive lung disease muscle weakness
A
lower TLC, higher RV (hard to blow air out), normal DLCO
8
Q
Extrapulmonary causes of restrictive lung disease
A
Chest wall (obesity), pleural disease, neuromuscular weakness
9
Q
Pulmonary causes of restrictive lung disease
A
Pulmonary edema, cardiogenic edema, pneumonia, lung injury/inflammation, ILD
10
Q
Pneumonia
A
infection in pulmonary parenchyma–initiates inflammatory response
11
Q
Pneumonia histology
A
- alveolar lumens filled with neutrophils and macrophages
- congested capillaries
- thickened alveolar walls
12
Q
Pneumonia causes
A
lower compliance lung from loss of aerated lung (exudate), atelectatic units, flood alveolar units (less participation in ventilation
13
Q
Lung inflammation causes
A
- autoimmune (lupus, scleroderma, rheumatoid arthritis)
- injury (aspiration, noxious inhalation, trauma)
- meds (methotrexate, blemycin, nitrofurantoin, amiodarone)
- hypersensitivity pneumonitis
14
Q
Lung inflammation results in
A
- widened alveolar septa
- increased elastic recoil forces (compliance decreases)
- increased work of breathing
- loss of alveolar/capillary units (obliterate capillary)
- hypoxemia
15
Q
Cardiogenic pulmonary edema pathophysiology (Restrictive lung disease)
A
Rising capillary hydrostatic forces cause:
- increase in interestitial edema
- overwhelm lymphatic drainage
- development of alveolar edema
**fluid is transudative (low protein, low cells)
16
Q
Cardiogenic pulmonary edema results in
A
- decreased compliance (interstitial water, flood alveolar units-no ventilation similar to pneumonia)
- hypoxemia
- activation of alveolar stretch receptors (J)-respond to increased interstitial fluid and stimulate ventilation (RR)
17
Q
ARDS (pulmonary edema due to damage to alveolar capillary membrane)
A
low pressure pulmonary edema-acute respiratory failure
- injury and disruption of membrane
- alveolar flooding with protein rich exudate
- severe hypoxemia
- reduced lung compliance
18
Q
Berlin definition ARDS
A
acute: within one week of known clinical insult
bilateral pulmonary infiltrates on CXR/CT
non cardiac reasons
hypoxemia P:F <300
19
Q
P:F ratio
A
ratio of PaO2 to FiO2, lower means worse oxygenation
20
Q
ARDS pathophysiology (acute)
A
initial injury to capillary endothelium/and or alveolar epithelium–leak alveolar capillary units and elaboration of protein rich cell rich exudates into alveolar space. Results in intense inflammatory reaction and deactivation of surfactant
21
Q
ARDS and Diffuse alveolar damage DAD
A
- alveolar septal thickening (edema and inflammation)
- hyaline membranes (proteinacious deposits in alveolar spaces, results from fibrin rich exudative fluid and necrotic epithelial cells )
- Type II cell hyperplasia to attempt repair
22
Q
Hypoxemia in ARDS
A
low PaO2
higher PAO2–leads to large Aa gradient
slight respiratory alkalosis (low PCO2, high pH) due to stimulation of ventilation from J receptors
23
Q
Acute hypoxemia respiratory failure AHRF in ARDS
A
airspace flooding (edema, pus, blood in alveoli) intrapulmonary shunt physiology-refractory to oxygen supplementation
24
Q
ARDS causes
A
- decreased lung compliance from flood and collapsed alveolar units 9surfactant dysfunction)
- interstitial edema/inflammation
- difficulty inflating/ventilating, loss of ventilated alveoli leads to over dissension and barotrauma
25
ARDS pathophysiology chronic
1. fibroproliferative phase: fibroblast proliferation and collagen deposition (scarring), Type II epithelial cell proliferation for repair, iniate resorption of exudate
Survivors: full reepitheliazation, endothelial restoration, resolution of scar formation (over months)
26
ARDS management
supportive care
lung protective ventilator strategy (low tidal volumes, permissive hypercapnia, limit alveolar distending pressure <30 cm H20, non toxic FiO2
27
Interstitial lung disease
disorders predominately affecting the interstitial space of the lung
primarily affects the lung parenchyma (alveolar/capillary units) with inflammation, fibrosis, architectural distortion
28
Common pathophysiology of ILDs
1. accumulation of inflammation and connective tissue in alveolar interstitial spaces of lung which causes
increased elastic recoil (low TLC, FRC ,RV)
destruction of alveolar/capillary gas surfaces (low DLCO and high Aa gradient)
thickening of alveolar capillary interface (diffusion limitation and exercise induced hypoxemia
29
Clinical findings in ILDs
```
dyspnea on exertion
fatigue
non productive paroxysmal cough
abnormal breath sounds (inspiratory crackles)
abnormal CXR CT (interstitial opacities)
hypoxemia
```
30
ILDs Idiopathic pulmonary fibrosis
most common form of idiopathic interstitial pneumonia
31
Idiopathic pulmonary fibrosis pathophysiology
1. induction of lung injury
2. tissue injury and response (inflammation)
3. abnormal wound healing
4. parenchymal fibrosis and architectural distortion
leads to decreased SA, VQ mismatch, hypoxemia, and breathlessness
32
Clubbing
seen in IPF, asbestosis, lung cancer, CF, less common in COPD
due to growth factors such as VEGf, PDGF
33
IPF diagnosis
usually 50+ age
1. exclude other causes (drug, environment, collage vascular disease)
2. exam shows inspiratory crackles and clubbed digits
3. UIP radiographic patern
4. PFTs show restriction, reduction in DLCO
5. surgical biopsy shows UIP
34
Usual Interstitial Pneumonia
irregular reticular lines (diffuse)
sub pleural, posterior, lower lobe predominance
sub pleural honeycombing
interlobular septa thickened by scarring
some normal areas of lung (heterogeneity)
loss of normal lung architecture/distortion
35
Acute exacerbation of IPF
acute SOB, new radiographic infiltrate, worsening gas exchange and no evidence of other causes (infection, HF, thromboembolism pneumothorax)
36
Disease course is variable in IPF
some people have faster progression than others, some have more exacerbations etc
37
IPF management
pirfenidone and nintedanib (inhibit fibrogenic pathways)
pulmonary rehab
supplemental O2
lung transplant for eligible patients
38
Pneumoconioses
accumulation of dust in lungs and the tissue reactions to its presence
results in nodular fibrosis and diffuse fibrosis
39
Abestos exposure
plumbing, sheet metal, shipbuilding, dockworkers, remodeling/demolition, mining, soils
40
Abestos related thoracic disease
Pleural disease: pleural plaques, benign asbestos pleural effusion, rounded atelectasis
```
malignant mesothelioma
bronchogenic carcinoma (asbestosis and smoking)
```
41
Abestosis pathophysiolgy
fibers are persistent and active-can lead to oxygen free radicals which injury tissue and slowly leads to fibrosis
long latency >20 years
42
Abestosis diagnosis
```
reliable history (exposure and latency)
evidence of interstitial lung fibrosis (crackles, clubbing, certified B reader for CT/CXR)
absence of other causes
```
43
Abestosis Chest CT
peripheral and basilar intersititial fibrosis and honeycombing (like UIP)
44
ferruginous bodies
asbestos coated fiber with iron, engulfed by macrophage, but they are rare, not required for dx
45
Benigng abestos pleural effusion BAPE
one of the first things to occur-short latency, not a precursor for mesothelioma. often bloody and eosinophilic, typically resolves
46
hyaline pleura plaques
most common CXR abnormality
usually asymptomatic
discrete areas of fibrosis/thickening of parietal pleura
47
rounded atelectasis secondary to pleural adhesions
usually asymptomatic comet tail sign on chest CT
48
Malignant mesothelioma
rare tumor from pleural or parietal mesothelium forming a mass or rind with associated effusion, not related to tobacco use. poor prognosis (6-18 mo)
49
Primary lung cancer
abestosis and smoking-need to quit smoking
50
Silicosis
inhaled and poorly cleared from UPPER lung zones
| chronic-upper lung nodules and mediastinal lymph nodes (egg shell calcifications)
51
Acute silicosis
short term high intensity exposure with latency of weeks to months
dyspnea, cough fatigue, alveolar filling with exude
52
Chronic silicosis
chronic exposure >5 years, latency >20 years, upper lobe nodules and egg shell calcifications of mediastinal lymph nodes
results in upper lobe fibrosis, restriction on PFT, dyspnea on exertion, progressive massive fibrosis
complicated by mycobacterial infections (TB), cor pulmonale, malignancy
53
Progressive massive fibrosis
found in chronic silicosis--basically obliterate the upper portion of the lung
54
Silicosis histology
```
pigment laden macrophages
cholesterol clefts
carbon deposits
pink collage
emphysema (associated with silicosis not sure why)
```
55
Silicosis tx
no proven therapies
| avoid exposure and stop smoking
56
Hypersensitivity pneumonitis
lung disease from recurrent exposure to ORGANIC particles, smaller than 5 microns--disease in very tiny bronchioles (bronchiolcentric)
57
HP antigens
farmer's lung (moldy why), hot tub, pigeon breeders, humidifier lung, spelunkers, cheese washers, industrial spray painters
58
Acute HP
rare presentation, associated with large exposure, mediated by immune complex deposition, fevers, chills, muscle aches, cough ,dyspnea, occasionally fine crackles
typically resolves on own
59
Chronic HP
chronic repetitive small exposures, dyspnea on exertion
cough, crackles (velcro) inspiratory squeaks early during inspiratory cycle
possible fibrosis on chest CT
poor prognosis
60
HP and PFTs
mixed obstructive/restrictive pattern
high RV
low FVC and FEV1
low FEV1/FVC
most common is isolated restrictio
61
Chronic HP on imagin
upper lobe predominant
diffuse bilateral reticule nodular pattern
ground glass opacities
areas of air trapping
62
HP with fibrosis imaging
honeycombing may be mid central (IN UIP IT IS LOWER AND PERIPHERAL)
63
HP pathology
poorly formed loose granulomas centered around small airways, multinucleated giant cells, diffuse mixed interstitial inflammation
64
HP dx
1. known exposure to inciting antigen (history, serologic IgG)
2. compatible clinical findings (crackles, cough, SOB, wheeze, fatigue, fever and CXR/CT findings)
3. bronchoalveolar lavage with lympocytosis
4. positive inhalation challenge (improve with removal or worsen with re exposure)
5. histopathology (surgical lung biopsy for granulomas and mononuclear cell infiltrate)
1,2,3 or 1,2,4 or 2,3,5
65
HP tx
avoid exposure, corticosteroids for acute events
steroid sparing agents (mycophenolate, mofetil, azathioprine, rituximab for progressive disease
lung transplant evaluation
66
Sympathetic activity
fight or flight, increase sweating, piloerector, send blood to muscles, pupils dilate, increase HR
67
parasympathetic activity
rest and digest, increase salivation, increase gut acitivy, pupil constriction, decrease HR
68
Sympathetic origins and path
T1-L2 cell bodies, short presynaptic to sympathetic chain ganglia, post ganglionic to organs and skin (glands) releasing AcH or NE.
divergence allows for faster whole body reaction
69
Parasympathetic origins and path
brainstem and S2-S4, long pre synaptic, synapse in terminal ganglia (no divergence), organs only and Ach only
70
Sympathetic preganglionic cell bodies
lateral horn of gray matter in T1-L2
71
Sympathetic chain
or sympathetic trunk-runs length of ENTIRE vertebral column, contain post ganglionic cell bodies
72
Communicating rami (white)
On ramp, have myelin, slightly more lateral, lead In to the sympathetic chain, located only on T1-L2, preganglionic only
73
Communicating rami (gray)
off ramp, no myelin, slightly more medial, lead OUT of sympathetic chain, post ganglionic fibers only, located in ALL spinal nerves
74
Splanchnic nerves
go to organs, exit anteriorly from sympathetic chain
75
Collateral ganglia
house post ganglionic cell bodies that are only going to innervate organs (not skin) located on anterior surface of aorta
76
autonomic plexuses
found in thorax and abdomen, follow blood vessels to destinations
77
Sympathetic innervation
```
T1-T3 head and salivary glands
T4-T6 heart, lungs, esophagus
T7-9 stomach liver, gall bladder, pancreas
T10-11 appendix, colon
T12-L2 rectum, bladder, uterus
```
78
Sympathetic pathway to skin and limbs
Cell bodies in lateral horn-->through ventral root-->through spinal nerve-->through white rami-->synapse in sympathetic chain-->post ganglionic leaves gray ramps-->exits via dorsal or ventral rami
T1-L2
79
Sympathetic pathway to thoracic organs
cell bodies in lateral horn-->through ventral root-->spinal nerve-->white rami-->sympathetic chain (NO SYNAPSE)-->on to the splanchnic nerve where it synapses-->post ganglionic through cardiopulmonary plexus
T1-T6
80
Sympathetic pathway to abdominal organs
Cell bodies in lateral horn-->exit via ventral root--> through spinal nerve-->white rami-->chain ganglion (NO SYN)-->thoracic splanchnic-->synapse in collateral ganglion-->travel via autonomic plexus to abdomen
T5-T12
81
Sympathetic pathway to adrenal medulla
cell bodies in lateral horn-->ventral root-->spinal nerve-->white rami-->ganglia-->thoracic splanchnic-->collateral ganglion-->chromatin cells (second neuron)
T8-L1
82
Parasympathetic nerves
CN III tears snot saliva
CN VII
CN IX
CN X vagus
83
Vagus nerve
left recurrent laryngeal, cardiopulmonary plexus (in between carina and left atrium), esophageal plexus, vagal trunks (left vagus-anterior and right vagus-posterior), autonomic plexuses to other organs
84
Pelvic splanchnics
hind gut and pelvic organs, lateral horn of S2-S4, exitvcia ventral rami (more in HFT)
85
autonomic dysreflexia
noxious stimuli like full bladder or bed sore causes a stress response (sympathetic)--sends up spinal cord but doesn't get to brain due to injury. However, autonomic reflexes will cause vasoconstriction in bottom half (increase BP). high BP sensed in aorta and carotid-top half sends signal to brain to decrease HR and BP.
emrgency
86
ANS myelin
little to none
| no myelin on post synaptic cells
87
Fetal circulation
very high pulmonary vascular resistance (low oxygen tension, low vasodilation, high vasoconstrictor) because we don't need blood going to lungs
foramen ovale and ductus arterioles shunt blood
88
Post natal circulation
reduction in PVR (alveolar oxygenation)
unless you have persistent pulmonary HTN of news born-PVR fails to drop
89
Normal pulmonary presures
RA: 0-7
RV 15-25 sys or 3-12 dia
PA 15-25 sys or 8-15 dia or 10-20 mean
PAOP 8-12
90
Pulmonary vascular resistance
PVR: mPAP-LAP/CO (x80 if doing dynes)
PVR decreases with rising CO because of recruitment and distention of capillaries
mPAP will rise with rising CO (mPAP=PVRxCO + LAP)
91
as SV increases, what is effect on RV and LV
RV has dramatic increase in pulmonary pressure because it can't handle the increased after load. LV is better adapted
92
Hypoxic pulmonary vasoconstriction
ALVEOLAR (not arterial) hypoxia controls vasoconstriction
93
mechanism of Hypoxic pulmonary vasoconstriction
small pulmonary arteries sense hypoxia and this inhibits K channels on smooth muscle cell leading to depolarization-->VCa channels let in Ca which increases myosin light chain phosphorylation and smooth muscle contraction.
inhibits perfusion to hypoxic areas and redirects to better ventilated areas
94
Pulmonary vasoconstrictors
Hypoxia, acidosis, hypoventilation, hypercarbia
so decreased pH is going to result in greater pulmonary vasoconstriction at same PO2
95
Pulmonary vasodilators
alkalosis, hyperventilation, oxygen, NO
96
humoral mediators of pulmonary pressure (vasoconstrictor)
endothelin 1, thromboxane A2, serotonin, angiotensin II
97
humoral mediators of pulmonary pressure (vasodilators)
prostaglandin I2, E2
oxygen
vasoactive intestinal peptide
98
Pulmonary hypertension
Mean PAP>25 mmHg at rest
usually high mortality from R heart failure
dyspnea, syncope, chest pain, edema
99
Causes of Pulmonary HTN
1. Idiopathic Pulmonary arterial HTN
2. left heart disease
3. lung disease and chronic hypoxia
4. chronic thromboembolic disease
100
Idiopathic pulmonary arterial hypertension
intimal, medial, adventitial thickening of muscular pulmonary arteries
pulmonary artreiits
concentric onion skinning
plexiform lesions
101
Pulmonary HTN due to left heart disease
systolic heart failure, diastolic heart failure, valvular disease, congenital anomalies of left ventricular outflow tract.
less common: restrictive pericarditis, infiltrative cardiomyopathy (sarcoid, amyloid)
left atrial enlargement/dilation results in passive venous congestion of Pulmonary veins--can lead to distension and vascular remodeling
102
PHTN mechanism in left heart disease
passive increase in mPAP (loss of LA compliance, diastolic dysfunction, etc) leads to endothelia dysfunction, decrease NO and increase ET, vasoconstriction, decreased BNP vasodilation (further increase mPAP) which leads to vascular remodeling which may cause RV failure and death
103
PH in left heart disease differentiation from PAH
MOST COMMON CAUSE of PHTN
differentiate via elevated left atrial pressure (PCWP)
104
Tx of PHTN LH dz
treat the left heart disease (Stent, ace inhibitors, HF drugs, diuretics)
105
PHTN due to lung disease/chronic hypoxemia
destroy lung parenchyma-lose vascular bed, stiffening of large pulmonary arteries, chronic hypoxia leads to medial hypertrophy and muscularizatin of small Pulmonary arteries, chronic inflammation leads to vascular remodeling
106
PHTN and lung disease/hypoxemia
second most common cause of PHTN
| typically only if you have severe disease (ILD IPF, COPD/emphysema, sleep disordered breathing
107
Tx of PHTN from lung disease
treat underlying disease, avoid vasoconstrictors (hypoxia)
avoid vasodilators bc you will vasodilate areas that don't ventilate well--messing with appropriate pulmonary hypoxic vasoconstriction
108
Chronic thromboembolic disease
loss of vascular surface area due to clot, more common if recurrent PE, microvascular remodeling similar to PAH
1 in 4 have no prior history of PE
requires lifelong anticoagulation
evaluate for surgical emoblectomy
109
Clinical presentation of PH
early-nonspecific dyspnea (60%), fatigue, chest pain, syncope
late-Right HF
nospecific labs-elevated BNP
CXR: enlarged PAs and RA/RV dilated
PFTs reduced DLCO but other will be normal
110
If it is purely HTN due to right heart failure, you will not have
crackles
111
Dx of PHTN
echo: primary screening test: look for PASP>35mmHg, LA/RA dilatation, tricuspid regard, RV hypertrophy, dysfunction
evaluate for cause:
1. LFT, ANA, HIV
2. ECHO (LHD)
3. PFTs, overnight
4. VQ scan
Right heart Cath is confirmatory!
112
Dx of Idiopathic pulmonary arterial hypertension
diagnosis of exclusion
more common in females, 30-50
elevated blood pressure in pulmonary arteries can reach systemic values
113
Tx of PAH
target the endothelin, NO, and prostacyclin pathways vasodilators and inhibition of pro proliferative response of pulmonary vasculature
114
Why does RH fail in PHTN?
low pressure system, thin muscular wall, not as adaptable to higher strain
115
Cor pulmonale
RV failure that develops from chronic pulmonary hypertension from pulmonary disorders
(primary pulmonary vascular problem or primary pulmonary airway/alveolar/parenchymal problem)
does not include RV failure secondary to LV failure
evidence of altered structure (hypertrophy or dilation) and impaird RV function
116
Cor Pulmonale most common caues
COPD, pulmonary fibrosis
117
Cor Pulmonale symptoms
progressive dyspnea, syncope, chest pain
118
Cor pulmonale exam findings
elevated JVP, loud S2, holosystolic murmer at left lower sternal border, hepatomegaly, ascites, lower extremity edema
common cause of hospitaliztion/death
119
Respiratory acidosis acute vs chronic
in acute: rise in PCO2 leads to small increase in HCO3, so pH decrease
in chronic: rise in PCO2 leads to large increase in HCO3, so pH normal
120
Respiratory alkalosis acute vs chronic
in acute: fall in PCO2 leads to small decrease in HCO3, so pH is elevated
in chronic: fall in PCO2 leads to large increase in HCO#, so pH is normal
**chronic alkalosis is very uncommon
121
Mild asthma attack values
low PaO2, low PaCO2, normal HCO3 and high pH
122
Moderate asthma attack values
more decrease in PaO2, decrease in PaCO2, normal HCO3 and high pH
123
Severe asthma attack value
very decreased PaO2, normal or elevated PaCO2, normal HCO3, normal or low pH
124
very severe asthma attack values
very very low PaO2, high PaCO2, high HCO3, very low pH
125
Early COPD values
decreased PaO2, normal or low PaCO2, Normal HCO3, normal or high pH
126
Late COPD values
lower PaO2, high PaCO2, high HCO3, normal or low pH
127
COPD exacerbation values
very very low PaO2, very very high PaCO2, higher HCO3, lower pH
Platelet and Bleeding Disorders
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